Presidential Address: Imagination trumps knowledge

• Published in: The American journal of surgery Vol. 200; no. 6; pp. 671 - 677
• Main Author: Moore, Frederick A., M.D
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2010; Elsevier Limited
• Subjects: Animals; Compensatory anti-inflammatory response; Enteral Nutrition; Gastrointestinal Tract - physiopathology; Gut ischemia-reperfusion; Humans; Inflammation; Inflammatory response; Ischemia; Mental task performance; Mortality; Multiple organ dysfunction syndrome; Multiple organ failure; Multiple Organ Failure - etiology; Multiple Organ Failure - physiopathology; Multiple Organ Failure - prevention & control; Nosocomial infections; Protein-Energy Malnutrition - complications; Protein-Energy Malnutrition - physiopathology; Reperfusion; Rodents; Sepsis; Surgery; Systemic inflammatory response; Systemic inflammatory response syndrome; Systemic Inflammatory Response Syndrome - etiology; Systemic Inflammatory Response Syndrome - physiopathology; Toxins; Trajectories; Translational Medical Research; Multiple organ failure; Systemic inflammatory response; Compensatory anti-inflammatory response; Enteral nutrition; Gut ischemia-reperfusion
• ISSN: 0002-9610; 1879-1883
• DOI: 10.1016/j.amjsurg.2010.05.009

Abstract Multiple organ failure (MOF) emerged 30 years ago and became our research focus. Over the years, we have proposed a series of cartoons that rallied multidisciplinary translational research teams around common themes to generate “win-win” hypotheses that when tested (right or wrong) have advanced our understanding of MOF. MOF has a bimodal trajectory, and the gut plays a role in both trajectories. Early MOF occurs because of excessive proinflammation (ie, systemic inflammatory response syndrome [SIRS]), and early gut ischemia-reperfusion can amplify SIRS and contribute to the early fulminant SIRS-MOF trajectory. Fortunately, most patients survive early SIRS, but some develop excessive anti-inflammation (ie, compensatory anti-inflammatory response syndrome). The gut also plays a role in this late indolent compensatory anti-inflammatory response syndrome–MOF trajectory. Multiple factors cause progressive gut dysfunction such that the gut (an important immunologic organ) worsens compensatory anti-inflammatory response syndrome and becomes the reservoir for pathogens and toxins that cause late sepsis.